© 2007 American Thoracic Society
Aging, the Aging Lung, and Senile Emphysema Are DifferentTo the Editor:In his recent editorial, Tuder implicated the pathophysiologic interrelationship between aging and cigarette smoke in the development of chronic obstructive pulmonary disease (COPD) (1). We believe that some of the points in this editorial are misleading. First, aging is a process leading to death and is characterized by universal progressive, deleterious, and irreversible alterations. But aging is not a disease. We can treat the age-related phenomena, but not aging itself. Tuder is commenting on the article by Sato and coworkers in the same issue, which is entitled "Senescence Marker Protein-30 Protects Mice Lungs from Oxidative Stress, Aging, and Smoking" (2). Sato and coworkers' title is incorrect. Importantly, previous studies have described physiologic changes of the lungs due to aging alone as aging lung or senile lung, but not as senile emphysema (3, 4). Here, the lungs were characterized as undergoing airspace enlargement without alveolar wall destruction (3, 4). Also, Janssens and coworkers' review, which was cited by Tuder, did not correctly differentiate the difference between aging lung and senile emphysema (5). Thus, age itself is known to be a risk for COPD, but not necessary for the development of COPD. Second, gene regulation of aging is complex. The master gene of aging has not been determined, although the Klotho gene is a candidate (6). Klotho gene–deficient mice develop the airspace enlargement without cigarette smoke exposure. Although mouse models of COPD often exhibited homogeneous alterations of lung structures, age-related changes of the lungs are heterogeneous in humans. The role of a single gene on the functional and morphologic changes of the lungs may be limited in humans. The redundancy of multiple genes associated with aging may substitute for the impaired cell function of lungs in humans due to a single gene defect. Third, there is no association of apoptosis and aging in human lungs. In particular, apoptotic cell death is not directly related to the aging process. Because apoptosis is an active process, it is not related to a degenerative process such as aging. We realized that the senescence marker protein-30 (SMP-30) gene is a good candidate gene for exploring the aging process and age-related diseases. However, the pathologic interaction between the aging process and COPD may not be solved by analyzing the SMP-30 gene and its protein products. We should differentiate physiologic aging, such as the aging/senile lung, from pathologic aging, as in senile emphysema (4). Furthermore, the resemblances and differences between senile emphysema and adult COPD should be better clarified.
University of Tokyo, Tokyo, Japan FOOTNOTES Conflict of Interest Statement: Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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